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相关概念视频

GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

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Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
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GPCR Desensitization01:12

GPCR Desensitization

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G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...
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TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
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G-Protein Gated Ion Channels01:21

G-Protein Gated Ion Channels

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GPCRs are primarily responsible for our sense of smell, taste, and vision.  The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
Sensory...
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Activation and Inactivation of G Proteins01:22

Activation and Inactivation of G Proteins

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Heterotrimeric G proteins are guanine nucleotide-binding proteins. As the name suggests, heterotrimeric G proteins are composed of three subunits: alpha, beta, and gamma. They remain GDP-bound or GTP-bound inside the cells and switch between inactive/active states. The Gα subunit possesses the nucleotide-binding pocket that binds guanine nucleotides and switches between GDP or GTP-bound states. In contrast, the Gꞵ and Gγ subunits are always bound together with high...
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Adrenergic Receptors: β Subtype01:26

Adrenergic Receptors: β Subtype

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β-adrenoceptors have varied sensitivities towards adrenaline, noradrenaline, and isoprenaline. The order of agonist potency is as follows:
Isoprenaline > Adrenaline > Noradrenaline
Neurotransmitter binding to these receptors causes activation of adenylyl cyclase resulting in increased concentrations of cAMP and modulation of calcium ion channels within the cell. They are further classified into β1, β2, and β3 subtypes.
β1-adrenoceptors: β1-adrenoceptors...
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相关实验视频

Updated: Jun 28, 2025

Quantitative Measurement of γ-Secretase-mediated Amyloid Precursor Protein and Notch Cleavage in Cell-based Luciferase Reporter Assay Platforms
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总体人参化物通过激活PPARγγ来降低Aβ的产生.

Shan He1, Junhe Shi2, Lina Ma2

  • 1Wangjing Hospital, China Academy of Chinese Medical Sciences, Beijing, China.

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
|April 9, 2024
PubMed
概括
此摘要是机器生成的。

人参中的总体人参化物 (TG) 改善记忆,减少阿尔茨海默氏症患者的粉样β (Aβ).

关键词:
阿尔茨海默氏症是阿尔茨海默氏症的一种疾病.粉样蛋白β 是一种蛋白质.在BACE1中获得了BACE1学位.在 NF-κBB 中.在PPARγ中,PPARγ是PPARγ

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Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons
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科学领域:

  • 神经科学是一个神经科学.
  • 药理学 药理学是指药理学的学科.
  • 生物化学 生物化学

背景情况:

  • 阿尔茨海默病 (AD) 是一种神经退行性疾病,其特点是粉样β (Aβ) 斑块的积累.
  • 从人参中提取的总体人参酸 (TG) 显示出对AD的潜在治疗益处.
  • 在AD中TG发挥作用的确切机制在很大程度上仍未确定.

研究的目的:

  • 阐明总金色化物 (TG) 在改善阿尔茨海默氏症 (AD) 病理方面的潜在机制.
  • 研究PPARγ在调解TG对粉样β (Aβ) 生产和认知功能的影响中的作用.

主要方法:

  • 使用了APP/PS1转基因小鼠和N2a/APP695细胞,分别作为体内和体外模型.
  • 使用莫里斯水迷宫 (MWM) 评估认知功能,并通过H&E和Nissl染色进行神经元变化.
  • 量化Aβ沉积,基因/蛋白质表达 (BACE1,PS1,PS2) 和NF-κB p65转位,采用免疫光学,西部涂抹和qRT-PCR.

主要成果:

  • 在APP/PS1小鼠中,TG治疗显著改善了空间学习和记忆.
  • TG的使用减少了小鼠在皮质和海马体中的Aβ积累.
  • 在细胞中,TG作为PPARγ激动剂,抑制NF-κB p65转位,降低Aβ1-40/Aβ1-42分泌和氨基基基因基因表达.

结论:

  • 总体人参化物 (TG) 在体内和体外都有效降低了粉样蛋白-β (Aβ) 的产生.
  • 通过TG激活PPARγ是促进Aβ清除和改善AD小鼠模型中的认知缺陷的关键机制.